Twelve female patients undergoing intermittent hemodialysis (HD) and 5 females posttransplantation (PT) were studied. All the HD patients had menstrual disturbances and 5 had galactorrhea. The mean basal LH level was significantly elevated (p less than .05) in patients on HD compared to normal controls, but the mean LH response to luteinizing hormone releasing hormone (LRH) was not significantly different from the control group. Mean basal FSH and the FSH response to LRH was normal. In the PT pateints the LH response to LRH was significantly greater at 120 min when compared to normal females. In the HD group the serum 17B estradiol, progesterone and testosterone levels were significantly lower than in the controls but in the PT group only testosterone levels were significantly lower. These results differ from those previously found in uremic males. Elevated prolactin levels were found in the patients on hemodialysis and correlated well with the presence of galactorrhea. These was no correlation between the elevated prolactin levels and amenorrhea in the patients on hemodialysis but one PT patient with amenorrhea had elevated prolactin levels.

The detoxification capacity of the liver in chronic active hepatitis (CAH) without liver cirrhosis (LC) is not sufficiently known. Therefore, we examined, in 156 patients with morphologically proven CAH of different stages, plasma ammonia, free phenols, indican, glucuronic acid and urea synthesis rate as parameters for liver detoxification. We found a significant increase of ammonia, phenols, and indican and a significant decrease of glucuronic acid and urea synthesis rate parallel to the stage of CAH without LC. In 34 CAH patients with complete recovery, a retrospective 10-year follow-up was possible. Parallel to the normalization of liver morphology and general liver tests, detoxification parameters also normalized. However, the detoxification disorders in CAH without LC are mild in nature and do not produce hepatic encephalopathy. Probably, they are caused by a reduced synthesis of the urea-cycle enzymes and of glucuronyltransferase in the liver.

The files of patients who underwent emergency endoscopy in a 2-yr period (January 1985 to January 1987) in the Heinz-Kalk Hospital were analyzed to establish the frequency, significance and therapy of the Mallory-Weiss syndrome associated with portal hypertension, an association observed in 55 of 339 patients (16.2%). Portal hypertension was caused by cirrhosis in 53 patients and by a prehepatic block in two patients. For 21 of these patients (37%) with portal hypertension, Mallory-Weiss syndrome was the first bleeding manifestation. They numbered 6.2% of the whole population. In the remaining 34 patients (63%) sclerotherapy treatment had been previously performed. No lesions that suggested peptic esophagitis were seen in these 55 patients, although in 25 of them (45.4%) a gastroesophageal reflux was observed. The frequency of bleeding from a Mallory-Weiss tear was significantly higher in patients with advanced liver disease, particularly with Child-Pugh classifications C and B. In patients with prehepatic block, a hemorrhage from a Mallory-Weiss tear may occur, but the frequency is significantly lower than it is in patients with cirrhosis. The bleeding tear was treated by transendoscopic esophageal and cardial wall sclerosis (paravariceal technique) and was, in all cases, successfully controlled. Mallory-Weiss syndrome is observed more frequently in patients with portal hypertension and cirrhosis. Gastroesophageal reflux apparently does not play a major role in the pathogenesis of this syndrome. It may simply be the manifestation of an abnormal gastroesophageal function. Mallory-Weiss syndrome can also be observed as a cause of rebleeding in patients treated with chronic sclerotherapy. Paravariceal endoscopic sclerotherapy is apparently the treatment of first choice to stop hemorrhage.